Wildlife are fed by humans intentionally or accidentally all over the world. This common activity can change wildlife physiology and behavior, intensify human-wildlife interactions, and influence human health through the transmission of infectious disease. This research will examine how feeding wildlife influences the spread of infectious disease, focusing on vampire bats and rabies virus. It will develop models that can a) forecast the future spread of rabies when livestock rearing expands into undisturbed habitats and b) predict human and animal rabies risk in areas undergoing rapid land conversion. Results could alter societal views on activities ranging from bird feeders to ecotourism and will directly improve predictions of the spread of a lethal disease. The project will support education and training of a doctoral student in modern molecular biology techniques and will develop new tools for evaluating disease in bats.
The research will integrate observed relationships between livestock abundance, antiviral immunity, and bat dispersal between colonies into mathematical models of rabies transmission. Earlier research showed that livestock rearing is associated with higher chronic stress, lower antibody levels, and larger vampire bat colonies, suggesting that livestock rearing produces source populations of immune-impaired vampire bats. The first research goal will use novel immunological tools on field-collected samples to characterize expression of antiviral cytokines of vampire bats across a livestock density site gradient in two regions. These data will be used to test if bats in livestock-dense habitat invest more or less in responses that promote resistance to rabies virus. The project's second goal will use molecular genetics approaches to characterize the connectivity of bat populations at fine spatial scales through field-collected tissue samples. Results will determine whether or not bat movement varies with livestock distribution. Finally, the researchers will develop a spatially explicit mathematical model of rabies transmission that incorporates results from the first two goals to provide a mechanistic framework for understanding how resource heterogeneity affects viral spread.
